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Journal articles on the topic 'Fetus Growth'

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Published: 4 June 2021
Last updated: 29 January 2023

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1

Kim, O. H., and K. S. Shinn. "Postnatal growth of fetus-in-fetu." Pediatric Radiology 23, no. 5 (September 1993): 411–12. http://dx.doi.org/10.1007/bf02011978.

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2

Pilliod, Rachel A., Jessica M. Page, Teresa N. Sparks, and Aaron B. Caughey. "The Growth-Restricted Fetus." Obstetrical & Gynecological Survey 74, no. 7 (July 2019): 383–85. http://dx.doi.org/10.1097/01.ogx.0000569524.58213.11.

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3

Denis, Danièle, Maud Righini, Claudie Scheiner, Françoise Voloty, L. Boubli, X. Dezard, J. Vola, and J. B. Saracco. "Ocular Growth in the Fetus." Ophthalmologica 207, no. 3 (1993): 117–24. http://dx.doi.org/10.1159/000310417.

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4

Denis, Danièle, Françoise Faure, Françoise Volot, Claudie Scheiner, L. Boubli, Xavier Dezard, and J. B. Saracco. "Ocular Growth in the Fetus." Ophthalmologica 207, no. 3 (1993): 125–32. http://dx.doi.org/10.1159/000310418.

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5

Shamsuddin, L., and A. K. M. Shamsuddin. "Growth pattern of Bangladeshi fetus." International Journal of Gynecology & Obstetrics 70 (2000): B30. http://dx.doi.org/10.1016/s0020-7292(00)86183-4.

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6

Harding, JE, and BM Johnston. "Nutrition and fetal growth." Reproduction, Fertility and Development 7, no. 3 (1995): 539. http://dx.doi.org/10.1071/rd9950539.

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Nutrient supply to the fetus is a key factor in the regulation of fetal growth. However, the direct supply of nutrients to provide building blocks for tissue growth is likely to be only a minor component of this regulation. The indirect effects of nutrition on fetal endocrine and metabolic status, and on the interaction between the fetus, placenta and mother all of which must be coordinated to allow fetal growth are also important. Maternal undernutrition may alter the growth of the fetus and its different component tissues in a way which cannot be explained solely on the basis of reduced substrate supply during the rapid growth phase of the tissues involved. Adaptation to altered substrate supply, during both undernutrition and refeeding, involves sequential changes in the metabolic and endocrine interactions between the fetus and the placenta. In addition, undernutrition has long-term consequences for the fetus. There is evidence for nutritional programming of fetal endocrine and cardiovascular systems before birth. Nutritional effects may also persist over more than one generation. The effects of nutrition on fetal growth are far more complex than simply those of substrate deprivation.
7

Hart-Elcock, Laura, R. D. Baker, and H. W. Leipold. "Growth of the Early Bovine Fetus." Journal of Veterinary Medicine Series A 37, no. 1-10 (February 12, 1990): 294–99. http://dx.doi.org/10.1111/j.1439-0442.1990.tb00908.x.

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8

Mathai, M., S. Thomas, A. Peedicayil, A. Regi, P. Jasper, and R. Joseph. "Growth pattern of the Indian fetus." International Journal of Gynecology & Obstetrics 48, no. 1 (January 1995): 21–24. http://dx.doi.org/10.1016/0020-7292(94)02237-2.

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9

Hema, Karumpuzha R., and Richard Johanson. "Management of the growth-restricted fetus." Obstetrician & Gynaecologist 2, no. 2 (April 2000): 13–20. http://dx.doi.org/10.1576/toag.2000.2.2.13.

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10

Robinson, J., S. Chidzanja, K. Kind, F. Lok, P. Owens, and J. Owens. "Placental control of fetal growth." Reproduction, Fertility and Development 7, no. 3 (1995): 333. http://dx.doi.org/10.1071/rd9950333.

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The placenta exerts its effects on the growth of the fetus from the beginning of pregnancy via metabolic and endocrine mechanisms. To achieve this, the placenta exchanges a wide array of nutrients, endocrine signals, cytokines and growth factors with the mother and the fetus. These exchanges modulate or programme fetal growth and development. This review concentrates on the function and structure of the placenta in humans and in animals, and the effects of experimental perturbation of placental size and function on fetal growth. The consequences for fetal growth of varying the abundance of peptides or, by deleting genes, insulin-like growth factors or cytokines, are also described. Maternal nutritional and hormonal state from as early as the first few days after fertilization, can influence the growth rate of the placenta and the fetus and also the length of gestation. Influences on placental development and their consequences will clearly have an impact on the placental control of fetal growth. Variations in the maternal environment and consequent perturbation of the metabolic and endocrine environment of the placenta and fetus are implicated as being responsible for the associations between prenatal growth of the placenta and its fetus and the subsequent risk of adult disease. The next challenge will be to determine the dominant influences at each stage of fetal and placental growth.
11

Cosmi, Erich, Tiziana Fanelli, Silvia Visentin, Daniele Trevisanuto, and Vincenzo Zanardo. "Consequences in Infants That Were Intrauterine Growth Restricted." Journal of Pregnancy 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/364381.

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Intrauterine growth restriction is a condition fetus does not reach its growth potential and associated with perinatal mobility and mortality. Intrauterine growth restriction is caused by placental insufficiency, which determines cardiovascular abnormalities in the fetus. This condition, moreover, should prompt intensive antenatal surveillance of the fetus as well as follow-up of infants that had intrauterine growth restriction as short and long-term sequele should be considered.
12

Owens, JA. "Endocrine and substrate control of fetal growth: placental and maternal influences and insulin-like growth factors." Reproduction, Fertility and Development 3, no. 5 (1991): 501. http://dx.doi.org/10.1071/rd9910501.

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Fetal growth is largely controlled by the interaction of the genome with the availability of oxygen and glucose and by endocrine responses to variations in their supply. Insulin-like growth factor II (IGF-II), and probably IGF-I, modulate fetal growth. Insulin and thyroid hormones are controlled by the supply of glucose and oxygen, respectively, and they influence fetal growth, partly via IGF-I. Circulating IGF-I and -II are controlled acutely and chronically by glucose availability to the fetus. The transfer of substrates from the mother to the fetus is determined by placental transfer capacity and by placental utilization of those substrates. The fetus controls the latter via its blood concentrations of oxygen and glucose and possibly IGF-I. In the mother, placental hormones and proteins, such as progesterone, placental lactogen, placental growth hormone and proteases, increase circulating IGFs and alter the stability and concentrations of IGF binding proteins. These changes may direct the metabolic and growth adaptation of the mother to pregnancy, which ensures an adequate flow of substrates to the developing fetus.
13

Tudehope, David I. "Neonatal aspects of intrauterine growth retardation." Fetal and Maternal Medicine Review 3, no. 1 (January 1991): 73–85. http://dx.doi.org/10.1017/s0965539500000450.

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The growth-retarded fetus is susceptible to intrauterine death, perinatal asphyxia and subsequently neonatal morbidity. Recent technical advances have only moderately increased the obstetrician's ability to recognize the fetus with intrauterine growth retardation (IUGR) prior to delivery, compared with two decades ago when less than one-third of such infants were identified before labour and delivery.
14

Morrison, Janna L., and Kimberley J. Botting. "Does a growth-restricted fetus have fewer cardiomyocytes than a normally grown fetus?" Expert Review of Obstetrics & Gynecology 7, no. 4 (July 2012): 301–3. http://dx.doi.org/10.1586/eog.12.30.

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15

Hiraoka, Takanori, Takafumi Kudo, and Yasuo Kishimoto. "Catecholamines in Experimentally Growth-Retarded Rat Fetus." Asia-Oceania Journal of Obstetrics and Gynaecology 17, no. 4 (May 24, 2010): 341–48. http://dx.doi.org/10.1111/j.1447-0756.1991.tb00284.x.

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16

Baschat, Ahmet A., and Chris R. Harman. "Antenatal assessment of the growth restricted fetus." Current Opinion in Obstetrics and Gynecology 13, no. 2 (April 2001): 161–68. http://dx.doi.org/10.1097/00001703-200104000-00011.

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17

Galan, Henry L. "Timing Delivery of the Growth-Restricted Fetus." Seminars in Perinatology 35, no. 5 (October 2011): 262–69. http://dx.doi.org/10.1053/j.semperi.2011.05.009.

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18

Gardiner, H., J. Brodszki, and K. Maršál. "Ventriculovascular physiology of the growth-restricted fetus." Ultrasound in Obstetrics and Gynecology 18, no. 1 (July 2001): 47–53. http://dx.doi.org/10.1046/j.1469-0705.2001.00436.x.

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19

Sims, D. G. "Doppler studies in the growth retarded fetus." BMJ 294, no. 6571 (February 28, 1987): 577. http://dx.doi.org/10.1136/bmj.294.6571.577-a.

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20

Whittle, M. J., and K. P. Hanretty. "Doppler studies in the growth retarded fetus." BMJ 294, no. 6572 (March 7, 1987): 644. http://dx.doi.org/10.1136/bmj.294.6572.644-a.

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21

Takeda, Y., M. Nakabayashi, and M. Iwashita. "Intrauterine Treatment of the Growth Retarded Fetus." Journal of Perinatal Medicine 18, s1 (January 1990): 108. http://dx.doi.org/10.1515/jpme.1990.18.s1.108.

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22

Vora, Neeta L., and Nancy Chescheir. "Delivery of the growth restricted preterm fetus." Lancet 385, no. 9983 (May 2015): 2126–28. http://dx.doi.org/10.1016/s0140-6736(14)62455-7.

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23

Mol, Ben. "Delivery of the growth-restricted preterm fetus." Lancet 386, no. 10001 (October 2015): 1336. http://dx.doi.org/10.1016/s0140-6736(15)00327-x.

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24

Bekedam, D. J., G. H. A. Visser, J. J. de Vries, and H. F. R. Prechtl. "Motor behaviour in the growth retarded fetus." Early Human Development 12, no. 2 (November 1985): 155–65. http://dx.doi.org/10.1016/0378-3782(85)90178-1.

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25

Maršál, Karel. "Physiological adaptation of the growth-restricted fetus." Best Practice & Research Clinical Obstetrics & Gynaecology 49 (May 2018): 37–52. http://dx.doi.org/10.1016/j.bpobgyn.2018.02.006.

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26

Syusyuka, V. G., N. G. Kolokot, and I. F. Belenichev. "Oxidative stress markers in pregnant women with fetus growth inhibition and their influence on results of labour process." HEALTH OF WOMAN, no. 8(144) (October 31, 2019): 48–52. http://dx.doi.org/10.15574/hw.2019.144.48.

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The objective: estimate the oxidative stress markers and their influence on result of labour process of pregnant women with fetus growth inhibition. Materials and methods. The complex examination of 63 pregnant women was made in term of 28–34 weeks of gestation and in dynamics (examination in 3–4 weeks). І group includes 33 pregnant women with fetus growth inhibition. Group ІІ was presented by 30 pregnant women without fetus growth inhibition. Markers of oxidative modification of proteins were analyzed in blood serum by means of spectrophotometric method and glutathione level was analyzed by fluorometric method. Variational and statistical processing of results was made using Statistica 13 – license standard application program packages for multidimensional statistical analysis. Results. Estimation results of markers of oxidative modification of proteins and glutathione level in pregnant women of group under investigation in dynamics indicate the progress of imbalance between oxidants and antioxidants among pregnant women with fetus growth inhibition compared to women without fetus growth inhibition (p<0.05). Such changes occur in conditions of lack of glutathione which level was significantly and statistically lower (p<0.05) in pregnant women with fetus growth inhibition. These results indicate intensification of oxidative modification of proteins together with decrease of reserve and adaptive abilities of antioxidant system of serum in the present group of pregnant women and it is the manifestation of oxidative stress. Pregnancy course and labour in case of women with fetus growth inhibition is characterized by rise of complication percentage that has negative effect both on rate of operative labour process and perinatal complications. Conclusions. Pregnancy course complicated by fetus growth inhibition is characterized by intensification of oxidative modification of proteins with decrease of reserve and adaptive abilities of antioxidant system of serum. These results indicate occurrence of oxidative stress in this group of women. It should be considered as one of the important links of pathogenesis of fetus growth inhibition. Course of labour among women with fetus growth inhibition is characterized by increase of complication rate that has direct influence on percentage rise of operative labour process under urgent indications. Condition of infants with growth inhibition at birth is characterized by significant and statistical decrease of average indicators under Apgar score and in case of estimation of anthropometric indicators it is characterized by significant and statistical (р < 0.05) decrease of weight-height parameters of newborns. Key words: pregnancy, fetus growth inhibition, oxidative modification of proteins, antioxidative system of protection, obstetric and perinatal complications
27

Kaku, Shoji, Fuminori Kimura, and Takashi Murakami. "Management of Fetal Growth Arrest in One of Dichorionic Twins: Three Cases and a Literature Review." Obstetrics and Gynecology International 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/289875.

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Progressive fetal growth restriction (FGR) is often an indication for delivery. In dichorionic diamniotic (DD) twin pregnancy with growth restriction only affecting one fetus (selective fetal growth restriction: sFGR), the normal twin is also delivered prematurely. There is still not enough evidence about the optimal timing of delivery for DD twins with sFGR in relation to discordance and gestational age. We report three sets of DD twins with sFGR (almost complete growth arrest affecting one fetus for ≥2 weeks) before 30 weeks of gestation. The interval from growth arrest to delivery was 21–24 days and the discordance was 33.7–49.8%. A large-scale study showed no difference of overall mortality or the long-term outcome between immediate and delayed delivery for FGR, while many studies have identified a risk of developmental delay following delivery of the normal growth fetus before 32 weeks. Therefore, delivery of DD twins with sFGR should be delayed if the condition of the sFGR fetus permits in order to increase the gestational age of the normal growth fetus.
28

Clifton, V., A. Osei-Kumah, N. Hodyl, N. Scott, and M. Stark. "036. SEX SPECIFIC FUNCTION OF THE HUMAN PLACENTA: IMPLICATIONS FOR FETAL GROWTH AND SURVIVAL." Reproduction, Fertility and Development 21, no. 9 (2009): 9. http://dx.doi.org/10.1071/srb09abs036.

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The placenta plays a central role in the development of the fetus by modulating the supply of nutrients and oxygen throughout pregnancy. We have identified that the placenta adapts to the presence of a maternal pathophysiology in a sexually dimorphic manner which results in differences in fetal growth. We have reported that the female fetus reduces her growth in response to chronic maternal asthma which ensures her survival in the presence of an acute asthma exacerbation. Conversely the male fetus continues to grow normally in the presence of maternal asthma but this is associated with a poor outcome in the presence of an acute exacerbation. We propose that the sexually dimorphic response of the fetus is derived from differences in placental adaptation to a pathophysiological condition. In the presence of a female fetus and maternal asthma, we have observed global gene changes in the placenta accompanied by significant alterations in microRNA expression. Downstream of these alterations we have observed differences in protein expression especially in relation to placental cytokines and the glucocorticoid receptor. In the presence of a male fetus there are fewer changes in global placental gene and microRNA expression, and we have observed no alterations in expression of placental cytokines or the glucocorticoid receptor. These differential adaptations ensure increased survival of the female fetus and continued growth of the male fetus in adverse conditions.
29

Ross,, J. C., P. V. Fennessey, R. B. Wilkening, F. C. Battaglia, and G. Meschia. "Placental transport and fetal utilization of leucine in a model of fetal growth retardation." American Journal of Physiology-Endocrinology and Metabolism 270, no. 3 (March 1, 1996): E491—E503. http://dx.doi.org/10.1152/ajpendo.1996.270.3.e491.

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Placental transport and fetal utilization of leucine were studied at 130 days of gestation in six control ewes and in seven ewes in which intrauterine growth retardation (IUGR) had been induced by exposure to heat stress. Leucine fluxes were measured during simultaneous intravenous infusion of L-[1-13C]leucine into the mother and L-[1-14C] leucine into the fetus. In the IUGR group, the following leucine fluxes, expressed as micromol/min/kg fetus, were reduced compared with control: net uterine uptake (3.44 vs. 8.56, P<0.01), uteroplacental utilization (0.0 vs. 4.7, P<0.01), fetal disposal rate (6.4 vs. 8.9, P<0.001), flux from placenta to fetus (5.0 vs. 7.1, P<0.01), direct transport from mother to fetus (1.6 vs. 3.4, P<0.01), flux from fetus to placenta (1.5 vs. 3.2, P<0.001), and oxidation of fetal leucine by fetus plus placenta (2.1 vs. 3.2, P<0.02). Uterine uptake, uteroplacental utilization, and direct transport were also significantly reduced per gram placenta. We conclude that maternal leucine flux into the IUGR placenta is markedly reduced. Most of the reduced flux is routed into fetal metabolism via a decrease in placental leucine utilization and a decrease in the leucine flux from fetus to placenta.
30

Shenai, Ashwini. "Hormones Influencing Growth of the Fetus: A Review." Research Journal of Pharmacy and Technology 8, no. 6 (2015): 749. http://dx.doi.org/10.5958/0974-360x.2015.00119.5.

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31

Murtazina, Nuriya I., Elena D. Lutsai, and Sofya V. Ershova. "Growth rate of thyroid gland in human fetus." Science and Innovations in Medicine 6, no. 2 (June 30, 2021): 4–7. http://dx.doi.org/10.35693/2500-1388-2021-6-2-4-7.

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Objectives to determine the thyroid gland growth rate in the intermediate fetal period of human ontogenesis. Material and methods. The thyroid glands of 60 male and female fetuses aged from 14 to 27 weeks were the subject of this research. The material was divided according to fetus age in three groups: Group I from 14 to 18 weeks, Group II from 19 to 22 weeks and Group III from 23 to 27 weeks. Results. The study revealed the increase in all dimensions of thyroid gland related to the increase of fetus age. During the intermediate fetal period of ontogenesis, the growth varied from 19% (for the anteroposterior isthmus size) to 59% (for the right lobe height). The thyroid gland growth rate for different sex groups varied between 24% and 60% in female fetuses, in male fetuses from 20% to 57%. Besides, the thyroid lobes and isthmus of female fetuses grew at a higher rate than those of the male fetuses. The uneven growth of the anatomical structure was also registered when comparing different age groups within the intermediate fetal period. The highest rate of thyroid gland growth was observed starting from the 22nd week of fetal life; until the 19th week the growth rate ranged between 7% (isthmus) and 25% (right lobe). The study of the thyroid gland growth rate in female and male fetuses in different age groups revealed identical tendencies involving the active growth of thyroid gland dimensions starting from the 22nd week.
32

Chard, T. "Hormonal control of growth in the human fetus." Journal of Endocrinology 123, no. 1 (October 1989): 3–9. http://dx.doi.org/10.1677/joe.0.1230003.

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33

Tyson, R. Weslie, and Barton C. Staat. "The Intrauterine Growth-Restricted Fetus and Placenta Evaluation." Seminars in Perinatology 32, no. 3 (June 2008): 166–71. http://dx.doi.org/10.1053/j.semperi.2008.02.005.

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34

Bahtiyar, Mert Ozan, and Joshua A. Copel. "Cardiac Changes in the Intrauterine Growth-Restricted Fetus." Seminars in Perinatology 32, no. 3 (June 2008): 190–93. http://dx.doi.org/10.1053/j.semperi.2008.02.010.

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35

BOTSIS, D., N. VRACHNIS, and G. CHRISTODOULAKOS. "Doppler Assessment of the Intrauterine Growth-Restricted Fetus." Annals of the New York Academy of Sciences 1092, no. 1 (December 1, 2006): 297–303. http://dx.doi.org/10.1196/annals.1365.027.

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36

Chareonsirisuthigul, Takol, Suchin Worawichawong, Rachanee Parinayok, Patama Promsonthi, and Budsaba Rerkamnuaychoke. "Intrauterine Growth Retardation Fetus with Trisomy 16 Mosaicism." Case Reports in Genetics 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/739513.

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Fetal trisomy 16 is considered uniformly lethal early in gestation. It has been reported to be associated with the variability of clinical features and outcomes. Mosaic trisomy 16 leads to a high risk of abnormality in prenatal cases. Intrauterine growth retardation (IUGR) is a common outcome of mosaic trisomy 16. Herein, we report on the case of Thai male IUGR fetus with trisomy 16 mosaicism. The fetal body was too small. Postmortem investigation of placenta revealed the abnormality including small placenta with furcated cord insertion and single umbilical cord artery. Cytogenetic study demonstrated trisomy 16 that was found 100% in placenta and only 16% in the fetal heart while other organs had normal karyotype. In addition, cardiac and other internal organs examination revealed normal morphology.
37

Denis, D., O. Burguiere, F. Oudahi, and C. Schemer. "Measurement of facial growth in the human fetus." Graefe's Archive for Clinical and Experimental Ophthalmology 233, no. 12 (December 1995): 756–65. http://dx.doi.org/10.1007/bf00184086.

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38

Fry, Gordon, Deborah Pittinaro, and Shirley Eberly. "Pulsatile versus continuous growth in the human fetus." American Journal of Obstetrics and Gynecology 191, no. 6 (December 2004): S167. http://dx.doi.org/10.1016/j.ajog.2004.10.492.

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39

Baschat, Ahmet Alexander. "Venous Doppler Evaluation of the Growth-Restricted Fetus." Clinics in Perinatology 38, no. 1 (March 2011): 103–12. http://dx.doi.org/10.1016/j.clp.2010.12.001.

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40

Abitbol, M. Maurice. "Growth of the fetus in the abdominal cavity." American Journal of Physical Anthropology 91, no. 3 (July 1993): 367–78. http://dx.doi.org/10.1002/ajpa.1330910309.

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41

Hyatt, Melanie A., Helen Budge, David Walker, Terence Stephenson, and Michael E. Symonds. "Ontogeny and Nutritional Programming of the Hepatic Growth Hormone-Insulin-Like Growth Factor-Prolactin Axis in the Sheep." Endocrinology 148, no. 10 (October 1, 2007): 4754–60. http://dx.doi.org/10.1210/en.2007-0303.

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The liver is an important metabolic and endocrine organ in the fetus, but the extent to which its hormone receptor sensitivity is developmentally regulated in early life is not fully established. Therefore, we examined developmental changes in mRNA abundance for the GH receptor (GHR) and prolactin receptor (PRLR) plus IGF-I and -II and their receptors. Fetal and postnatal sheep were sampled at either 80 or 140 d gestation, 1 or 30 d, or 6 months of age. The effect of maternal nutrient restriction between early gestation to midgestation (i.e. 28–80 d gestation, the time of early liver growth) on gene expression was also examined in the fetus and juvenile offspring. Gene expression for the GHR, PRLR, and IGF-I receptor increased through gestation peaking at birth, whereas IGF-I was maximal near to term. In contrast, IGF-II mRNA decreased between midgestation and late gestation to increase after birth, whereas IGF-II receptor remained unchanged. A substantial decline in mRNA abundance for GHR, PRLR, and IGF-I receptor then occurred up to 6 months. Maternal nutrient restriction reduced GHR and IGF-II receptor mRNA abundance in the fetus, but caused a precocious increase in the PRLR. Gene expression for IGF-I and -II were increased in juvenile offspring born to nutrient-restricted mothers. In conclusion, there are marked differences in the ontogeny and nutritional programming of specific hormones and their receptors involved in hepatic growth and development in the fetus. These could contribute to changes in liver function during adult life.
42

WARSHAW, JOSEPH B. "Intrauterine Growth Retardation: Adaptation or Pathology?" Pediatrics 76, no. 6 (December 1, 1985): 998–99. http://dx.doi.org/10.1542/peds.76.6.998.

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Intrauterine growth retardation can result from a variety of environmental or genetic influences on fetal growth.1 The sequelae of intrauterine growth retardation resulting from impairment of nutrient flow from mother to fetus are well known and include low birth weight with sparing of brain growth, polycythemia, and hypoglycemia resulting from decreased storage fuels and defective gluconeogenesis. Despite the generally held assumption that nutritionally related intrauterine growth retardation (either maternal malnutrition or impaired uteroplacental blood flow) represents a serious pathologic insult to the fetus, the available data suggest that the vast majority of infants with intrauterine growth retardation have normal development without significant differences in IQ or neurologic scores from normal infants.2
43

Khajuria, Ruchi, and Megha Sharma. "Histopathology of placenta in intrauterine growth restriction (IUGR)." International Journal of Research in Medical Sciences 7, no. 3 (February 27, 2019): 889. http://dx.doi.org/10.18203/2320-6012.ijrms20190943.

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Background: Birth of healthy term baby depends on normal placenta. IUGR is a condition associated with placental insufficiency. There is a close relationship between IUGR and placental qualitative changes. The aim of the present study was to evaluate the morphological and histological changes in placentas of IUGR fetuses and in placentas of normal uncomplicated pregnancies and to determine the relationship that exists between morphological change and frequency of IUGR.Methods: In a cross sectional study conducted in the department of Pathology, GMC Jammu, a total of 60 placenta were received, 30 placenta of IUGR fetus (group 1-case) and 30 placenta of uncomplicated pregnancy with normal single fetus (group 2-control). Exclusion criteria: Twin pregnancy, gestational hypertension, diabetes, congenital anomaly, antepartum hemorrhage and systemic disorder.Results: Placental weights in IUGR group were significantly lower than control group. Average placental weight in IUGR group was 425 gms while in the control group (normal placenta) it was 550 gms. Infarction, intervillous thrombosis, chorionic villitis, hemorrhagic endovasculitis, placental intravascular thrombi, perivillous fibrin deposition, fibrinoid necrosis and villous edema were found to be more common in IUGR group (Group 1-case group) than Normal (Group 2- control group).Conclusions: This study highlightened that significant pathological differences were found between the placentas of IUGR fetus and normal fetus. The gross and microscopic measurement of a placenta is a good way to get proper information about IUGR and helps in management of the pregnancy.
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Parkes, M. J., and J. M. Bassett. "Antagonism by growth hormone of insulin action in fetal sheep." Journal of Endocrinology 105, no. 3 (June 1985): 379–82. http://dx.doi.org/10.1677/joe.0.1050379.

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ABSTRACT Insulin, glucose, lactate and alpha-amino acid nitrogen concentrations were measured in the plasma of ewes and their hypophysectomized fetal lambs during intravenous infusions of GH, prolactin or saline into the fetus in utero. Prolactin and saline had no effect on mother or fetus. Infusion of GH at 1·2 mg/kg per day for 2 days or at 0·4 mg/kg per day for 4 days caused a sustained twofold increase in the level of insulin and a smaller, but sustained, increase in the level of glucose in fetal plasma. We suggest that GH antagonizes the action of insulin in the fetus. Glucose supplies to the fetal brain and placenta may be protected by such antagonism of insulin use during glucose shortage. J. Endocr. (1985) 105, 379–382
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Gou, Chenyu, Xiangzhen Liu, Xiaomei Shi, Hanjing Chai, Zhi-ming He, Xuan Huang, and Qun Fang. "Placental Expressions of CDKN1C and KCNQ1OT1 in Monozygotic Twins with Selective Intrauterine Growth Restriction." Twin Research and Human Genetics 20, no. 5 (August 14, 2017): 389–94. http://dx.doi.org/10.1017/thg.2017.41.

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CDKN1C and KCNQ1OT1 are imprinted genes that might be potential regulators of placental development. This study investigated placental expressions of CDKN1C and KCNQ1OT1 in monozygotic twins with and without selective intrauterine growth restriction (sIUGR). Seventeen sIUGR and fifteen normal monozygotic(MZ) twin pairs were examined. Placental mRNA expressions of CDKN1C and KCNQ1OT1 were detected by real-time fluorescent quantitative PCR. CDKN1C protein expression was detected by immunohistochemical assay and Western-blotting. In the sIUGR group, smaller fetuses had a smaller share of the placenta, and CDKN1C protein expression was significantly increased while KCNQ1OT1 mRNA expression was significantly decreased. The CDKN1C/KCNQ1OT1 mRNA ratio was lower in the larger fetus than in the smaller fetus (p < .05). In the control group, CDKN1C protein expression showed no difference between larger and smaller fetuses, while KCNQ1OT1 mRNA expression was significantly lower in the larger fetus, and the CDKN1C/KCNQ1OT1 mRNA ratio was higher in the larger fetus than in the smaller fetus (p < .05). Our findings showed that pathogenesis of sIUGR may be related to the co-effect of the up-regulated protein expression of CDKN1C and down-regulated mRNA expression of KCNQ1OT1 in the placenta.
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Yakovleva, O. V., I. E. Rogozhina, and T. N. Glukhova. "Modern concepts of low birth weight and fetal growth restriction." Kazan medical journal 102, no. 3 (June 10, 2021): 347–54. http://dx.doi.org/10.17816/kmj2021-347.

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The aim of this work is to study the state of the problem of the development of small-for-gestational-age fetus and fetal growth restriction over the past 5 years. A review of randomized trials of the PubMed database for the period of 2015 to 2020 was carried out. Experts reached an agreement on the definition of diagnostic criteria for small-for-gestational-age fetus and fetal growth restriction, a clinically valid classification was created, and the main monitoring strategies were developed. Due to the different pathogenesis, fetal growth restriction is divided into early and late. The observation algorithm includes tests that have shown higher sensitivity and specificity. There is no single standard for the median weight and abdominal circumference of a fetus, indicators of the reference range for fetal Doppler. Smoking cessation and taking acetylsalicylic acid at a dose of 150 mg at high risk of preeclampsia is recommended to prevent the small-for-gestational-age fetus and fetal growth restriction. The pregnancy management algorithm includes Doppler ultrasound examination of the umbilical artery, cardiotocography. If this pathology occurs before 32 weeks of pregnancy, the blood flow in ductus venosus is additionally examined, and after 32 weeks of pregnancy, the middle cerebral artery blood velocities and cerebroplacental ratio are assessed. Indicators of Doppler velocimetry and cardiotocography, which serve as criteria for early termination of pregnancy, are developed, measures are proposed to improve neonatal outcomes prevention of respiratory distress syndrome at 2434 weeks of gestation, as well as magnesium therapy for fetal neuroprotection. The problems of preventing fetal growth restriction and the algorithm for monitoring pregnant women who do not have risk factors for small-for-gestational-age fetus, management tactics and indications for delivery while slowing fetal weight gain remain unresolved.
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SCHLABRITZ-LOUTSEVITCH, NATALIA, CUN LI, and PETER W. NATHANIELSZ. "INSULIN-LIKE GROWTH FACTORS AND PLACENTAL FUNCTION." Fetal and Maternal Medicine Review 18, no. 3 (August 2007): 201–24. http://dx.doi.org/10.1017/s0965539507001994.

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Placentas from different species differ not only in their cellular structure and normal trajectory of growth but also in the architecture of their placental vasculature and the transport and exchange mechanisms that determine nutritional transfer from mother to fetus and waste disposal from fetus to mother.1 Many maternal and fetal hormonal and nutritional factors, as well as placental paracrine and autocrine systems affect placental growth and development throughout gestation.2 Nutrients delivered from the maternal circulation are as important for placental growth as they are for fetal growth. In addition to passing across the placenta to provide the building blocks for fetal growth, amino acids, carbohydrate and lipids are incorporated into the placenta.
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Jensen, EC, JE Harding, MK Bauer, and PD Gluckman. "Metabolic effects of IGF-I in the growth retarded fetal sheep." Journal of Endocrinology 161, no. 3 (June 1, 1999): 485–94. http://dx.doi.org/10.1677/joe.0.1610485.

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It has been shown that IGF-I has an anabolic effect in the normal fetus. However, there is evidence to suggest that there may be IGF-I resistance in the growth retarded fetus. Therefore, we investigated the effects of acute IGF-I infusion to chronically catheterised fetal sheep. At 128 days gestation, fetuses underwent a 4 h infusion of IGF-I (50 microg/kg/h). Three groups of animals were studied. Nine normally grown fetuses were studied as controls. Embolised animals (n=8) received microspheres into the uterine vasculature, and animals with spontaneous intra-uterine growth retardation (IUGR animals) (n=6) were fetuses found at post mortem to be spontaneously growth restricted. The effects of IGF-I infusion on feto-placental carbohydrate and protein metabolism were similar in our control group to previous similar experiments. IGF-I infusion decreased fetal blood glucose, oxygen, urea and amino-nitrogen concentrations, and inhibited placental lactate production. The same fetal blood metabolite concentrations also fell during IGF-I infusion in the embolised fetuses, but the effect on placental lactate production was not seen. The only effect of IGF-I infusion in the spontaneous IUGR animals was a fall in fetal blood amino-nitrogen concentrations. We conclude that fetal IGF-I infusion does not have the same anabolic effects in the growth retarded fetus as the normal fetus. In addition, the effects of IGF-I were different in the two growth retarded groups. Our data support previous evidence that the growth retarded fetus has altered IGF-I sensitivity, and this may vary depending on the cause, severity and duration of growth retardation.
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Parveen, Shahista, Rohan Mascarenhas, Akhter Husain, and Devadas Acharya. "Prenatal and postnatal growth: An ultrasound and clinical investigation." APOS Trends in Orthodontics 6 (May 30, 2016): 147–53. http://dx.doi.org/10.4103/2321-1407.183150.

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Background Understanding facial development requires sound knowledge of growth at different stages. Although studies in the past have established the relationship between prenatal and postnatal growth, little research has been done using noninvasive ultrasound. The purpose of this study is to evaluate correlation between prenatal and postnatal growths using ultrasound as a fetal growth assessment tool. Study Settings: It is a hospital-based study where prenatal growth is measured at different intervals of gestational period and compared with the growth at birth. Materials and Methods: Ten subjects with normal pregnancy were studied using ultrasound. Cephalocaudal growth gradient, body proportions of the fetus were assessed and compared at different stages. Growth was also evaluated at birth and compared with the predicted growth. Results The growth rate of estimated fetal weight is at maximum between the 28th and 32nd week of the fetal life (P ≤ 0.001). The growth rate of head circumference, occipitofrontal diameter, and femur length is maximum between the 20th and 28th week of the fetal life (P < 0.001). Cephalocaudal growth gradient decreases with increased age of the fetus. Conclusions Prenatal growth is correlated with postnatal growth. Ultrasound can be used as a tool for the measurement and prediction of prenatal and postnatal growths.
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Clifton, V. L. "009. The effect of maternal asthma during pregnancy on placental function, fetal growth and childhood development." Reproduction, Fertility and Development 17, no. 9 (2005): 65. http://dx.doi.org/10.1071/srb05abs009.

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Fetal growth and neonatal birth weight are significant contributing factors to the development of adult disease states in later life. In human pregnancy, we have identified sexually dimorphic differences in fetal growth with the female fetus reducing growth in response to maternal asthma and the male fetus continuing to grow at a normal rate but being at an increased risk of in utero death. The physiological mechanisms that confer sex-specific differences in the fetal response to maternal asthma are unknown. However our research has identified differences in mechanisms associated with fetal glucocorticoid regulation, which are also associated with changes in childhood growth patterns. Asthmatic and control pregnant women were recruited at their first antenatal visit and followed through to delivery. Subjects were assessed for severity of asthma and their use of medication, including glucocorticoid therapy, was recorded. In addition to routine antenatal care, fetal growth was determined using Doppler ultrasound. Following delivery placentas and cord blood were collected. The children of the women followed during the study were examined by a paediatrician at 6 months of age and every 12 months after that initial visit. Our data shows that in response to maternal asthma, the female fetus has an increase in cortisol, which downregulates placental GR expression, immune and hypothalamic-pituitary-adrenal function and is associated with decreased growth. The male fetus responds to increased cortisol with an increase in GR expression and no change in HPA or immune function or growth. These data indicate that the male and female fetus have different strategies to control growth and in their response to a maternal stress, such as asthma.
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